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Stenotic Arteriosclerotic Coronary Artery Disease


Definition

Stenotic atherosclerotic coronary artery disease (CAD) is narrowing of the coronary arteries caused by thickening and loss of elasticity of their walls (arteriosclerosis) that, when sufficiently severe, limits blood flow to the myocardium. Initially, the disease limits only coronary flow reserve (increase in flow that normally accompanies increased myocardial oxygen demands), but when sufficiently advanced, CAD reduces blood flow through the affected artery even at rest. In its most severe form, atherosclerotic CAD occludes the coronary artery.

Historical Note

Development of coronary cineangiography by Sones and Shirey at the Cleveland Clinic during the early 1960s made possible direct identification of stenotic and occlusive atherosclerotic lesions in the coronary arteries during life and laid the foundation for coronary artery surgery. Sporadic surgical attempts to improve coronary blood flow had previously been made, but these efforts were ineffective because of lack of precise anatomic diagnosis. In 1951 in Montreal, Vineberg and Miller reported direct implantation of an internal thoracic artery (ITA), also known as the internal mammary artery (IMA), into the myocardium. More than a decade later, the Cleveland Clinic group demonstrated that this procedure brought new blood to the left ventricular (LV) myocardium, but the new blood flow was too limited in quantity and distribution to be effective. In 1954, Murray and colleagues were considering a direct surgical approach to CAD and reported experimental studies of anastomosing the ITA to a coronary artery. Shortly thereafter, Longmire and colleagues at the University of California in Los Angeles reported a series of patients in whom direct-vision coronary endarterectomy was performed without cardiopulmonary bypass (CPB). Subsequently, CPB was used to facilitate the operation, and Senning reported patch grafting of a stenotic coronary artery in 1961. At about this time, Effler and colleagues at the Cleveland Clinic began their pioneering efforts to achieve myocardial revascularization by a direct surgical attack on stenotic coronary lesions, as demonstrated by Sones using coronary angiography.

Largely overlooked is the first operation for CAD by Kolesov in Leningrad in 1964, in which the ITA was anastomosed to the left anterior descending coronary artery (LAD). Probably without knowledge of this contribution, in May 1967, Favaloro and Effler at the Cleveland Clinic began performing reversed saphenous vein bypass grafting, and by January 1971, this group had performed 741 such operations. Even earlier, Garrett, at that time working with DeBakey in Houston, successfully performed a reversed saphenous vein coronary artery bypass graft to the LAD in an unplanned way ; at restudy 7 years later, the vein graft was patent.

Progress was rapid after this early era. In 1968 in New York, Green and colleagues re-reported anastomosing the distal end of the left ITA to the LAD using a dissecting microscope, and Edwards and colleagues began using this procedure at UAB in 1969. In Milwaukee in 1971, Flemma, Johnson, and Lepley described the technique and advantages of sequential grafting , in which one vein was used for several distal anastomoses. Advantages of this technique were further amplified by the reports of Bartley, Bigelow, and Page in 1972 and Sewell in 1974. Bilateral ITA grafting was performed at least by 1972 and probably as early as 1968. Thus, within a very short time, the foundations were laid for rapid worldwide adoption of coronary artery bypass grafting (CABG).

Morphology

Development of Coronary Artery Stenosis

Atherosclerosis, the most common form of arteriosclerosis, is a process that in coronary arteries, as in other blood vessels, consists of focal intimal accumulations of lipids, complex carbohydrates, blood and blood products, fibrous tissue, and calcium deposits, as well as associated changes in the media. Lipoid foci are associated with or converted into plaques of fibrous or hyaline connective tissue, although at least some atherosclerotic plaques may result from organization of thrombi.

Fibrolipoid plaques may become thick enough to encroach on the lumen of the artery, producing a stenotic lesion. Probably episodically and at times over a period of years, new material is deposited on the luminal side of the plaque, resulting in further narrowing and sometimes complete coronary occlusion. Small blood vessels form around and within the plaque. Gradual regression of plaque enlargement, seen clinically as regression of stenoses in a few patients, and development of collateral coronary blood flow can result in at least partial spontaneous restoration of antegrade regional myocardial blood flow.

Hemorrhage may occur suddenly within a plaque (see “ Atherosclerotic Plaque Rupture and Thrombosis ” later in chapter); occasionally this may suddenly increase the degree of coronary stenosis and precipitate acute myocardial infarction (MI) or unstable angina pectoris. Thrombosis occasionally complicates the coronary atherosclerotic process, generally when there is luminal narrowing. Sudden complete obstruction may result, and it is generally agreed that acute thrombotic occlusion is the genesis of acute MI in most patients. Rapid recanalization frequently follows this process. Platelet aggregation within the lumen of an already narrowed coronary artery may induce thrombosis or suddenly narrow the lumen and provoke an acute MI or unstable angina, and it may play a role in development of the atherosclerotic plaque itself. Platelet aggregation releases thromboxane A 2 , an extremely potent vasoconstrictor. Thus, interrelationships among atherosclerotic narrowing, platelet aggregation, and coronary spasm are important.

The atherosclerotic process usually affects multiple coronary arteries. In 1975, Gensini reported that 40% of patients with CAD sufficient to lead to cineangiographic study had important stenoses in all three major coronary arteries, and in 30% two vessels were involved. Ninety-five percent of patients with complete occlusion of one artery had important stenoses in at least one of the other two arteries.

Atherosclerotic CAD usually involves the proximal portion of the larger coronary arteries, particularly at or just beyond sites of branching. Thus, stenoses in the main trunks of the LAD, circumflex (Cx) coronary artery, and right coronary artery (RCA) often involve the first of the secondary branches (first diagonal branch of LAD, obtuse marginal branch of Cx artery, and posterior descending branch of RCA). When CAD is more extensive in the main trunks, origins and first portions of secondary branches may be involved. Diffuse distal disease severe enough to render the patient unsuitable for CABG is uncommon. In 10% to 20% of patients with atherosclerotic CAD, the left main coronary artery is importantly stenotic.

Occasionally, a major coronary artery may lie beneath a muscle bridge. This is most common in the middle third of the LAD, but sometimes one or all of the obtuse marginal branches of the Cx artery are buried in muscle throughout their course. These portions of artery are typically free of severe atherosclerotic changes.

Myocardial Infarction and Morphologic Sequelae

When myocardial blood flow is sufficiently impaired in relation to myocardial oxygen demands, myocardial necrosis occurs. The resultant infarction may be subendocardial —that is, not involving the entire thickness of the ventricular wall, but only the inner third. In its most extreme form, subendocardial infarction may be diffuse and result from multiple-system disease. More often, however, subendocardial infarcts are regional and result primarily from a stenotic lesion in one or two systems. These infarcts are generally less extensive than so-called transmural infarcts, but still have serious implications. A transmural MI involves the entire thickness of the ventricular wall. Transmural infarction usually results from a sudden increase in luminal narrowing or complete obstruction of the artery supplying that area, or a sudden generalized increase in myocardial oxygen demand in the presence of a severely stenotic coronary artery. Although categorization of acute infarctions as subendocardial or transmural is convenient, most transmural MIs are not homogeneous but contain islands of viable muscle of varying number and size.

The process of infarction is complex. Animal studies indicate that some myocardial cells die after 20 minutes of complete coronary artery occlusion, and that extensive myocardial cell death occurs after 60 minutes. Although these time frames may vary, some reperfusion generally occurs within the ischemic area of myocardium within minutes of onset of acute ischemia, particularly in the zone between ischemic and nonischemic myocardium (border zone). If this spontaneous reperfusion occurs within 3 to 4 hours, the amount of necrosis is limited, at times substantially, infarct size is reduced, and mortality is decreased. The process is complex because, in addition to these beneficial effects, spontaneous reperfusion can result in hemorrhage, edema, and ventricular electrical instability.

Healing of the acute MI leaves a scarred area of myocardium. In most cases, this area is a mixture of fibrous tissue and viable myocardial cells in varying proportions. Such scarring is evident from (1) intraoperative inspection of areas of previous infarction at the time of CABG and (2) change from akinesia or dyskinesia to hypokinesia or normal wall motion in some LV wall segments when patients go from a symptomatic to an asymptomatic state after percutaneous coronary intervention (PCI) or CABG. When the scar is almost all fibrous tissue, it is usually large, and the LV wall may become akinetic or aneurysmal (see Chapter 8 ).

These morphologic changes may be self-aggravating because of their effect on circulation to the subendocardial layer. Repeated infarctions may occur and add still more scarring. In the aggregate, myocardial scarring leads to LV systolic and diastolic dysfunction and, ultimately, if the patient survives long enough, to the syndrome of chronic heart failure with elevated right atrial and jugular venous pressure, hepatomegaly, and fluid retention. More often, however, patients with severe ischemic LV dysfunction die of another infarction or ventricular fibrillation.

Atherosclerotic Plaque Rupture and Thrombosis

Several studies have emphasized the dynamic nature of coronary atherosclerotic plaque as a fundamental feature of CAD. Fissuring , or rupture, of atherosclerotic plaques is probably the genesis of the acute coronary syndromes termed unstable angina and acute MI . When this occurs, mural or occlusive coronary thrombi often coexist and contribute further to development of the unstable states.

Coronary stenoses that produce less than 50% reduction in lumen diameter are often the site of the atherosclerotic plaque rupture that precipitates unstable angina or acute MI. More severe stenoses also undergo plaque rupture, and total vessel occlusion may occur. However, an acute ischemic episode does not always develop, possibly because severely stenotic lesions are long-standing and have stimulated development of a protective collateral circulation.

Certain atherosclerotic plaques appear to have a higher risk of rupture than others. These plaques are characterized by relative softness, a high concentration of cholesterol and cholesterol esters, and a lipid pool that tends to be situated eccentrically. Rupture is through the cap of the plaque, and areas in which the cap lacks underlying collagen support seem particularly vulnerable.

Clinical Features and Diagnostic Criteria

Routine Methods

CAD is usually first suspected with development of the symptom complex of angina pectoris or an acute MI, occasionally because of electrocardiographic (ECG) evidence of a silent acute MI, a positive ECG response to a graded exercise test, or sudden death with resuscitation. Occasionally, CAD is first suspected because of cardiomegaly and symptoms of chronic heart failure without any other obvious cause.

The precise nature, location, duration, and severity of any chest pain are determined by carefully questioning the patient. Precipitating causes and maneuvers that relieve the pain are noted, as are any recent changes in pain pattern. Findings on physical examination are usually nonspecific.

Many noninvasive tests, beginning with a chest radiograph and ECG at rest and during exercise and then proceeding to more complex studies, are currently used to identify and quantify CAD and its sequelae. Such tests cannot yet define extent or distribution of anatomic coronary disease with great accuracy. From a surgical standpoint, therefore, properly performed coronary angiography remains the definitive diagnostic procedure (see “ Coronary Angiography ” in text that follows). Contrast-enhanced computed tomographic coronary angiography (CTCA) is emerging as a promising technique for detecting coronary artery disease (see “ Computed Tomographic Angiography ” later in this section) and may, with increased spatial and temporal resolution, be suitable as an accurate and noninvasive method to select candidates for CABG. Methods of evaluating LV function are also necessary. These may be based in part on historical data, physical findings, and chest radiography. Noninvasive and invasive special study methods may be used. Even when complex study methods are employed, results must be interpreted with knowledge of the simple but reliable clinical data. An ejection fraction (EF) of 35% has a different implication when accompanied by minimal LV enlargement seen on a chest radiograph than when enlargement is marked. An EF of 30% is much more ominous when accompanied by important elevation of jugular and right atrial pressure with hepatomegaly and fluid retention than when these pressures are normal. Exercise capacity may be variable in patients with similar EFs, and the variations are prognostically important. It should be emphasized, however, that heart size can be deceptive because it can remain normal in the presence of severe LV dysfunction.

Important associated conditions such as hyperlipidemia, arterial hypertension, and diabetes, and a history of MI, smoking, or a particularly stressful occupation or lifestyle should be noted. Because arteriosclerosis is the cause of CAD, its presence elsewhere in the circulatory system should be sought. A history suggesting transient cerebral ischemic attacks or stroke, particularly when carotid bruits are present, must be carefully pursued. A history of intermittent claudication and presence of diminished femoral, popliteal, or pedal pulses are indicative of peripheral arterial occlusive disease. The thoracic and abdominal aorta are examined for possible aneurysm or occlusive disease. Renal and pulmonary function should also be evaluated.

Coronary Angiography

Coronary angiograms provide important information. Their quality must be sufficient to permit detailed assessment from several angles of both coronary ostia and all major and minor branches of the left and right coronary arterial systems. However, angiography remains an imperfect method. Severity of a visualized stenotic lesion may be underestimated, and diameter of vessels distal to a stenosis is often underestimated.

Assessment of coronary arteries at operation by external palpation or probing of the open vessel cannot substitute for coronary angiography. When the arteries cannot be adequately filled by contrast media, however, or the available study is incomplete and cannot be repeated (this should be uncommon), intraoperative observations can be used to supplement angiographic findings. The surgeon should assess all coronary arterial branches carefully at the time of operation, rather than assume the coronary angiogram is a totally accurate diagnostic tool.

Recording and Reporting Data

Whatever the techniques used for coronary angiography, methods of recording and analyzing the data are crucial. A 75% cross-sectional area loss (50% diameter) is considered an important but moderate stenosis, and a 90% cross-sectional area loss (67% diameter) is considered severe ( Fig. 7-1 ). Some groups consider only those lesions with 70% or more diameter loss (90% or more cross-sectional area loss) as important, but an appropriately documented basis for this has not been established.

Figure 7-1, Diagrammatic representation of relationship between two methods of estimating severity of coronary artery stenosis.

Extent of important coronary artery stenoses has conventionally been summarized as “single-vessel,” “double-vessel,” or “triple-vessel” disease, usually with left main coronary artery disease as a separate category. This chapter uses the terms single-system, two-system , and three-system disease, because each coronary system (LAD, Cx, and RCA) consists of several vessels. Use of the term system is therefore more accurate than vessel .

These classifications have been criticized because they give no indication of the amount of LV myocardium rendered ischemic by the lesions. For example, a stenosis in the LAD system has a different significance when it lies at the origin of a large first diagonal artery than when it involves the middle third of the LAD beyond its major septal and diagonal branches, or only the first portion of a large first diagonal branch. A single stenosis in the proximal portion of the Cx artery varies in significance depending on whether this artery is dominant. Single-system disease involving the proximal RCA has a different implication from that involving only the posterior descending branch of the RCA. Many other examples can be given of the inadequacies of these classifications.

A few classification systems have been described to circumvent these limitations. These include Gensini's old and rather complex scheme that takes into account severity of the stenoses, the various segments of the coronary artery tree involved, and the area of myocardium usually perfused by them ; a simple scheme from Massachusetts General Hospital ; and the method of the Coronary Artery Surgery Study (CASS) of the U.S. National Heart, Lung, and Blood Institute (NHLBI), dividing the coronary arteries into a total of 27 specified segments. Some myocardial jeopardy scores have attempted to provide similar information but are limited by the assumption that akinetic areas cannot be revascularized.

Whatever the recording and reporting methods, they are not a substitute for the surgeon critically reviewing cineangiograms before deciding for or against operation, and again immediately before operation.

Computed Tomographic Angiography

Although conventional coronary angiography remains the gold standard to determine extent and severity of CAD and indications for CABG, CTCA using 64-slice multidetector CT scanners (MDCT) has been evaluated as an alternative method to select patients for CABG ( Fig. 7-2 ).

Figure 7-2, A-C, Multidetector computed tomographic volume rendering images show significant stenoses of major coronary arteries (arrows) , suggestive of three-system disease. These coronary lesions (arrows) were confirmed on conventional coronary arteriography (D-E), and patient underwent coronary artery bypass grafting. Key: LAD, Left anterior descending coronary artery; LCx, left circumflex coronary artery; RCA, right coronary artery.

Initial studies suggest that this technique is a suitable alternative to conventional coronary angiography in selected patients. However, concerns regarding exposure to excessive radiation and the small but defined increased risk of cancer in later life associated with exposure to radiation may limit its widespread application.

Coronary Intravascular Ultrasound

Intravascular ultrasound (IVUS) uses a high-frequency miniaturized ultrasound transducer positioned on the tip of a coronary artery catheter to provide detailed cross-sectional images of the coronary vessel wall ( Fig. 7-3, A ). Unlike coronary angiography, which details only luminal encroachment, IVUS provides images of the atherosclerotic plaque, characterizes its composition, and assesses severity of stenosis ( Fig. 7-3, B ). When compared with formalin-fixed and fresh histologic specimens of coronary arteries, it correlates significantly ( P < .0001) with coronary artery cross-sectional area ( r = 0.94), residual lumen cross-sectional area ( r = 0.85), and percent cross-sectional area ( r = 0.84). It is useful in determining the need for CABG in situations when the severity of coronary artery stenosis cannot be precisely determined by angiography, particularly for left main and LAD disease ( Fig. 7-3, C ).

Figure 7-3, Coronary intravascular ultrasound (IVUS). A, Schematic of IVUS catheter within blood vessel, cross-sectional imaging plane, and resultant image. Transducer types are shown. B, Vessel wall thickness assessed by IVUS imaging. Mild (left, arrows) and moderate (right, arrows) amounts of intimal thickening are shown. C, Angiographic underestimation of disease. Although angiogram (top) shows only mild luminal irregularities, two sites in left anterior descending coronary artery (arrows) show major arteriosclerosis by IVUS (below) .

Coronary Artery Pressure and Fractional Flow Reserve

Fractional flow reserve (FFR) is a simple, reliable, and reproducible physiologic index of lesion severity in patients with intermediate stenosis, and is another method to determine the need for CABG and PCI in equivocal situations, particularly stenosis of the left main coronary artery. The concept of FFR is illustrated in Fig. 7-4 . Pressure measured distal to the stenotic coronary lesion during maximum hyperemia (Pd) divided by mean aortic pressure (Pa) correlates with maximum myocardial blood flow in the presence of a stenosis divided by the normal maximum myocardial blood flow . FFR 0.75 to 0.80 or less is generally an indication for intervention.

Figure 7-4, Concept of fractional flow reserve (FFR). Key: P a , Mean aortic pressure; P d , hyperemic distal coronary pressure; , normal maximal myocardial blood flow; , maximal myocardial blood flow in the presence of a stenosis.

Left Ventricular Function Testing

Resting and Exercise Tests

Because resting LV function is presumed to depend on the amount of myocardium that is free of scar, severity of LV dysfunction may be a surrogate for amount of myocardial scar. This may not be entirely accurate in patients with ischemic heart disease, because ischemia may result in myocardial stunning or hibernation and reversible depression of at least systolic LV function (see “Myocardial Cell Stunning” in Chapter 3 ). CABG and PCI do not favorably affect myocardial scarring.

Exercise LV function in patients with ischemic heart disease is characteristically depressed; this reflects loss of coronary flow reserve imposed by the distribution and severity of CAD. Amount of decrease in EF or other measures of the heart's response to stress is a surrogate for the distribution and severity of coronary arterial stenoses.

Systolic and Diastolic Function

LV function can be expressed as systolic or diastolic function. Systolic function is determined by contractility of the ventricle (see “Cardiac Output and Its Determinants” in Section I of Chapter 5 ). Diastolic function describes compliance, or extensibility, of the ventricle, which is related to preload.

Global and Segmental Function

Global LV function is usually described by an index of overall ventricular systolic function, most often EF. EF is not independent of preload or afterload and therefore is not an ideal index, but it is the one most frequently used and is reasonably satisfactory. EF is obtained commonly and least accurately by visual estimation from a cineangiographically recorded left ventriculogram, more accurately (and originally) by quantitative angiography, and also by noninvasive methods such as radioisotopic imaging and echocardiography.

The CASS score was developed by CASS investigators as a measure of global LV function and actually is a summation of five segmental wall scores based on wall motion observed in the right anterior oblique (RAO) projection of the cineangiogram. Table 7-1 shows the relationship between EF and CASS scores. Other scoring systems have also been developed.

Table 7-1
General Interrelations Among Modifiers Describing Left Ventricular Dysfunction, Ejection Fraction, and Coronary Artery Surgery Study Score
LV Dysfunction EF CASS Score (Normal = 5)
< Ratio ≤ < Score ≤
None .60 5
Mild .50 .60 5 9
Moderate .35 .50 9 15
Severe .35 15
Key: CASS, Coronary Artery Surgery Study; EF, ejection fraction; LV, left ventricular.

Segmental wall function refers to function, usually systolic, of segments of the LV wall. Methods usually depend on observation of wall motion or wall thickening throughout the cardiac cycle. Analysis of segmental wall motion is particularly informative in patients who have previously sustained MIs.

Load-Independent Function

High LV afterload tends to depress LV systolic function and therefore cardiac output, and high LV preload generally increases cardiac output (see “Cardiac Output and Its Determinants” in Section I of Chapter 5 ). Methods previously discussed generally do not reflect load-independent LV function and are therefore suboptimal.

Natural History

Gaps exist in knowledge of the natural history of atherosclerotic CAD. Many of these gaps will be permanent because withholding treatment is no longer justifiable. The closest approach to natural history comes from data gathered in patients seen and treated medically before about 1970. Unfortunately, many studies from that era have the disadvantage that patients were not categorized according to anatomic extent of their disease and LV function.

A further complexity is that in nearly all studies since 1970, patients initially undergoing no treatment or medical treatment have properly been allowed thereafter to cross over to interventional treatment (PCI or CABG). This has made it even more difficult to generate accurate information about the natural history of CAD.

Stenotic Coronary Artery Disease

The natural history of patients with a given severity and distribution of CAD depends in part on the rate of progression of both. As an added complexity, regression of some lesions also occurs. In general, however, both severity and distribution of CAD tend to increase with time, although the rate of increase is highly variable and difficult to predict. In general, over a 2-year period in patients with already important stenoses, 20% of the stenoses increase in severity, and about half of patients develop important new lesions. The mechanism of increase in severity is variable, but atherosclerotic plaque rupture and thrombosis play important roles in some cases (see “ Atherosclerotic Plaque Rupture and Thrombosis ” earlier in this chapter).

Of the usually accepted risk factors for presence of stenotic CAD, not all have been helpful in predicting its rate of progression. Aggressiveness of the atherosclerotic process seems to be a risk factor for progression; surrogates for it include young age at presentation with symptomatic CAD, peripheral arterial disease, diabetes, and hyperlipidemia. Nature of the atherosclerotic plaque is a risk factor because plaque rupture is frequently the inciting incident leading to progression in severity of coronary artery stenosis. Eccentric positioning of the lipid pool within the plaque appears to predispose to rupture and thus progression in severity of stenosis. Rheologic factors play a role; the more severe the stenosis, the more rapid the progression toward total occlusion.

Left Ventricular Dysfunction

Stress-Induced Dysfunction

First indications of LV dysfunction in patients with ischemic heart disease are localized abnormalities of regional wall motion (LV systolic function) during exercise or other forms of stress. These abnormalities are the result of transient myocardial ischemia, which can be demonstrated as myocardial perfusion defects during exercise.

Global LV systolic function improves during exercise in normal persons, except in old age. By contrast, when initially localized areas of myocardial ischemia become sufficiently extensive, global LV systolic function declines during exercise. Exercise-induced ECG changes also reflect these reversible myocardial perfusion abnormalities, which may be so severe as to cause hypotension during exercise testing. Related to this exercise-induced decrease in function in some patients, LV end-diastolic volume responds abnormally to exercise by increasing, often to more than 50% above resting value. These reversible abnormalities of regional myocardial perfusion and wall motion occasionally occur at rest, most often in patients with unstable angina.

Abnormalities of LV diastolic function during stress can be demonstrated in most patients with extensive CAD. These abnormalities take the form of reduced peak LV filling rate and increased time to peak filling rate. These phenomena are the clinical reflection of the laboratory demonstration that ischemia impairs rate of diastolic relaxation of papillary muscle, related to the fact that myocardial relaxation during early diastole is an active, energy-dependent process. Abnormalities of diastolic function in patients with coronary artery stenoses may also reflect lack of an increase in early diastolic coronary blood flow.

In the aggregate, these purely ischemic abnormalities of LV systolic and diastolic function may be severe enough during stress to result in a considerable increase in LV end-diastolic pressure. This may produce dyspnea and even transient paroxysmal nocturnal dyspnea and pulmonary edema, as well as angina, during severe ischemic episodes. Further evidence that these abnormalities of LV systolic and diastolic function can result from myocardial ischemia alone is provided by their reversal after successful PCI or CABG.

Dysfunction at Rest

LV dysfunction with the patient at rest and under no stress has been considered the result of myocardial scar. Therefore, it can be expected that it will not improve after neutralization of the coronary arterial stenoses by CABG or PCI. However, there is evidence that myocardial stunning or hibernation, or both, may be responsible at times for considerable LV dysfunction, and that this element of resting LV dysfunction can be relieved by revascularization.

Myocardial scars from previous MIs also result in abnormalities of LV diastolic function. Both clinical and experimental studies indicate that increase in LV end-diastolic volume, which results from both diastolic and systolic abnormalities of function, is directly related to the amount of scar in the ventricle.

Patients whose LV function is depressed from myocardial scarring exhibit morphologic, physiologic, and functional variability. Some have moderately increased LV end-diastolic pressure at rest and a considerably reduced exercise capacity but only a mildly increased cardiac size on chest radiography. These patients have moderate scarring and marked ischemic dysfunction in scarred or non-scarred parts of the ventricles that can often be improved by revascularization. Some have chronic symptoms of pulmonary venous hypertension and may still be helped by revascularization. A few have moderate or severe cardiomegaly, reduced cardiac output, importantly elevated right atrial and jugular venous pressure, hepatomegaly, and fluid retention. Patients in the latter group have advanced LV dysfunction from extensive myocardial scarring, and it generally cannot be improved by operation unless the scar is discrete, is full thickness (aneurysmal or akinetic), and can be resected (see Chapter 8 ).

Unfavorable Outcome Events

Stable Angina

Development of chest discomfort or pain on exertion is common in patients with coronary artery stenosis, but chest discomfort is not an inevitable accompaniment of even important CAD. Severity of angina is typically categorized by the Canadian class system, which differs from the New York Heart Association (NYHA) classification for heart failure.

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    Class I: angina occurring only with strenuous or prolonged exertion at work or recreation and not with ordinary physical activity (thus, Class 0 means no angina under any circumstance).

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    Class II: angina occurring with walking rapidly on level ground or a grade and with rapidly walking up stairs. Ordinary walking for fewer than two blocks on level ground or climbing one flight of stairs does not cause angina except during the first few hours after awakening, after meals, under emotional stress, in the wind, or in cold weather. This implies slight limitation of ordinary activity.

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    Class III: angina occurring when walking fewer than two blocks on level ground at a normal pace, under normal conditions, or when climbing one flight of stairs. This implies marked limitation of ordinary physical activity.

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    Class IV: angina occurring with even mild activity. It may occur at rest but must be brief (<15 minutes) in duration. (If the angina is of longer duration, it is called unstable angina .) This implies inability to carry out even mild physical activity.

Angina generally results from reduction in coronary flow reserve in a portion of the myocardium; the more severe the reduction, the greater the severity of angina. However, severity of angina also depends on amount of stress or exercise, which increases myocardial oxygen demand in proportion to the intensity of the activity. Standardization of demand gives graded exercise testing its advantage in quantifying to some extent the amount of “reversible ischemia” (more properly, the amount of reduction of coronary flow reserve). Absence of angina does not eliminate the possibility that the patient has “reversible ischemia.” Although angina tends to become more severe as time passes, a number of patients do not experience this trend.

Unstable Angina

Unstable angina undoubtedly signifies a prognostically important change in the coronary circulation, but the syndrome takes so many different forms that its precise definition has been difficult. Not surprisingly, different practitioners and even different randomized trials have used different definitions. In 1989, Braunwald devised a classification system to ensure uniformity of categorization and provide diagnostic and prognostic information.

Although “unstable angina” implies several syndromes, no differences in outcome have been identified among its subgroups. The term applies to patients with severe and persisting angina on presentation to the physician or hospital, with ECG evidence of ischemia and only minor enzymatic evidence (available only later) of MI. The syndrome is considered more ominous if it occurs in the absence of stimuli that increase total body oxygen consumption or catecholamine release (e.g., unusual emotional stress, fever, infection, hypotension or uncontrolled hypertension, tachyarrhythmia, hypoxemia). Unstable angina also applies to patients who have onset of severe angina (Canadian class IV) within 2 months of presentation or who have recurring or prolonged (>15 minutes) severe angina within 10 days of presentation, whether or not it is of new onset. The term is also appropriate for patients who develop (or continue to have) severe angina in the first 2 weeks after an acute MI. All subsets usually demonstrate ECG evidence of myocardial ischemia during severe pain, and no enzymatic evidence of more than minimal myocardial necrosis.

The cause of unstable angina is now considered to be an acute change in coronary circulation with or without changes in related neurohumoral responses. Unstable arteriosclerotic plaque, which may fissure and rupture, is the genesis of unstable angina in many patients (see “ Arteriosclerotic Plaque Rupture and Thrombosis ” earlier in this chapter). However, superimposed thrombosis and platelet aggregation complicate local situations, and the clinical state largely depends on activity of the patient's thrombolytic state and mechanisms for reversing platelet aggregation. The process is reversible but tends to recur either as another episode of unstable angina or as an acute MI.

Acute Myocardial Infarction

Prevalence of acute MIs in patients with coronary artery stenoses is not known precisely, but it is surely affected by prevalence of risk factors. For example, patients with severe proximal LAD lesions have a particular tendency to develop acute and often fatal MI. Among patients who are sufficiently symptomatic and undergo coronary angiography, at least 10% have an acute MI within 1 year, 30% within 5 years, 40% within 10 years, and 50% within 15 years, as determined from patients assigned to initial medical treatment in the Veterans Administration (VA) randomized trial of stable angina.

Acute MI is usually caused by acute subtotal or total occlusion of the vessel supplying the infarcted region, and the vessel usually does not have well-formed collateral arteries. This fact has been suspected for many years and gave rise to the early phrase “coronary thrombosis.” However, thrombosis was first convincingly demonstrated by DeWood and colleagues in Spokane, Washington, in a series of patients undergoing emergency CABG for acute infarction. Often the acutely occluded vessel has not previously had a severe stenosis, which is consistent with the concept that the myocardium supplied by the diseased vessel is usually devoid of important collateral vessels. Current information suggests that rupture of an unstable arteriosclerotic plaque is the genesis of the acute reduction in luminal diameter, often accompanied by thrombosis and platelet aggregation (see “ Arteriosclerotic Plaque Rupture and Thrombosis ” earlier in this chapter).

The greater the number of MIs, the greater the likelihood the patient will have another one, which may indicate that some people generate more unstable plaques than others. Also, the more coronary artery systems (LAD, Cx, RCA) that contain important stenoses, the greater the probability of an acute MI. This may simply be due to the increased number of coronary arteriosclerotic plaques available to rupture.

Early (3-month) mortality after acute MI is difficult to define for the current era. Hospital mortality is usually described, but the early phase of the hazard function continues for about 3 months. In the past, hospital mortality in a heterogeneous group of patients admitted with acute MI was 10% to 50%, depending on prevalence of risk factors. Death was usually in acute or subacute cardiac failure, or suddenly with ventricular fibrillation. Size of the infarct was an important risk factor; hospital mortality was 5% for patients with small infarcts vs. 50% for those with large infarcts (involving 40% or more of LV mass). Reserve in the adjacent “nonischemic” myocardium appeared also to relate to probability of surviving an acute MI, indicating the importance of metabolically supporting this area and revascularizing it even if the stenoses are not severe. Overall probability of death was higher after the second infarction and still higher after the third, related to scarring imposed by previous infarctions. Development of pulmonary edema soon after acute MI increased risk of death, but 1-year mortality was as low as 10% when other risk factors were favorable.

Currently, therapy is directed toward use of inhibitors of platelet aggregation, thrombolytic agents, heparin, and PCI as soon as possible after onset of infarction. Although the optimal protocol may be arguable, effectiveness of this therapy is not. Hospital mortality has been reduced to about 7% to 10% by these measures. When cardiogenic shock develops, emergency PCI or CABG with maximal measures for myocardial management can salvage many patients (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ).

Death

Approximately 70% to 80% of a heterogeneous group of patients with CAD of sufficient severity to cause them to seek medical advice ultimately die a cardiac death. The remaining 20% to 30% die of unrelated causes. Overall survival for a heterogeneous group of patients with clinically evident CAD is 75% at 5 years after initiation of medical treatment, 60% at 10 years, and 45% at 15 years. However, time-related probability of death in a group of CAD patients is so related to prevalence of risk factors that overall estimates are of little value.

Most often, death occurs with acute or subacute cardiac failure, often within a few months of an acute MI and sometimes precipitated by a ventricular arrhythmia. Infrequently, death is attributable to chronic heart failure, either late after one or more infarctions or without any identifiable earlier episode of infarction. This mode of death is generally characterized by a slow downhill course, eventually leading to hepatomegaly, ascites, and ultimately death. Death in this mode is usually the direct result of myocardial scarring.

About 20% of patients with important CAD who have had no interventional therapy die suddenly. Acute MI is not the only cause of sudden death. Presumably, sudden cardiac death in patients with ischemic heart disease can result from acute, severe myocardial ischemia, resulting in ventricular fibrillation, asystole, or acute severe depression of ventricular function.

Incremental Risk Factors for Unfavorable Outcome Events

Understanding the benefit of interventional therapy, whether CABG or PCI, demands a knowledge of the incremental risk factors for unfavorable outcome events in patients treated medically for CAD.

Multivariable analysis is used to generate incremental risk factors for various unfavorable events after CABG, PCI, or medical treatment. However, those identified are often surrogates for more basic risk factors, and at times several surrogates for the same basic risk factors appear. Box 7-1 presents the basic risk factors as currently perceived. In the future, these factors themselves may become more clearly identifiable.

Box 7-1
Incremental Risk Factors for Death and Other Unfavorable Outcome Events in Patients with Stenotic Atherosclerotic Coronary Artery Disease a

a Factors/events listed are not the result of a formal multivariable analysis, but rather a composite of many such analyses.

  • Severity of Reduction in Regional Coronary Flow Reserve b

    b These categories constitute reversible ischemia.

    • Angina severity (Canadian class I to IV)

    • Degree of positive response to stress testing

    • Severity and number of stenoses

  • Number of Myocardial Regions with Reduced Coronary Flow Reserve b

    • Left main stenosis and severity

    • Distribution and severity of coronary stenoses

    • Myocardial score

  • Nature of Coronary Arteriosclerotic Plaque

    • Number of previous myocardial infarctions

    • Acute myocardial infarction

    • Distribution of coronary stenoses

  • Internal Milieu (Thrombotic or Fibrinolytic)

    • Number of previous myocardial infarctions

    • Acute myocardial infarction

    • Distribution of coronary stenoses

  • Aggressiveness of Atherosclerotic Process

    • Diffusely narrowed coronary arteries

    • Peripheral arterial disease

    • Cerebrovascular disease

    • Hyperlipidemia

    • Diabetes

    • Hypertension

    • Younger age at intervention

  • Rate of Progression of Coronary Arterial Stenoses

  • Amount and Distribution of Myocardial Scar

    • Number of previous acute myocardial infarctions

    • Left ventricular ejection fraction

    • Left ventricular Coronary Artery Surgery Study (CASS) score

    • Left ventricular end-diastolic pressure

    • Defects identified by exercise or resting thallium-201 scintigraphy (delayed or after reinjection)

  • Secondary Conditions

    • Hemodynamic instability

    • Cardiogenic shock

    • Ischemic instability (unstable angina)

    • Ventricular electrical instability

  • Coexisting Conditions (Comorbidity)

    • Older and younger age

    • Larger and smaller body size

    • Ethnicity

    • Diabetes

    • Hyperlipidemia

    • Hypertension

    • Chronic pulmonary disease

    • Chronic renal disease

    • Smoking

    • Previous stroke

Reduced Regional Coronary Flow Reserve

Reduced regional flow reserve results from severity of the coronary arterial stenoses and number of coronary arterial systems with important stenoses. The left main coronary artery is an additional “system.”

Time-related survival for a heterogeneous group of patients with single-system stenosis is high, approximately 90% to 95% at 5 years ( Fig. 7-5, A ). At 15 years, survival is about 50%. Additional risk factors relating to reduction in regional coronary flow reserve include (1) specific vessel(s) diseased, (2) location of stenosis within the vessel, and (3) severity of stenosis. Because time-related mortality from single-system disease is relatively low, the differences attributable to further refinements in this category will be small and therefore difficult to identify. Also, inferences from the analyses are only as good as reliability of the cineangiogram.

Figure 7-5, Survival of medically treated men with coronary artery disease, stable angina of at least 6 months’ duration, and less than severe left ventricular dysfunction enrolled in the U.S. Veterans Administration (VA) Cooperative Study (solid squares). R3 For comparison, survival is shown of a population matched for age and gender from the 1976 U.S. life tables (solid line). Data for other groups of medically treated patients published earlier by Burggraf, B67 Oberman, O2 and Webster W4 and their colleagues are also shown. Lower survival in the last three groups may have been the result of less restrictive selection of patients than for the VA group and better medical treatment in the more recent VA group. Data from the Coronary Artery Surgery Study (CASS), in which important stenosis meant a 70% diameter reduction, are also presented. M27 These data include patients treated medically in the current era with all types of ventricular function. Left main coronary artery data from CASS refer to left main coronary artery plus triple-system disease. A, Single-system disease. B, Two-system disease. C, Three-system disease. D, Left main coronary artery disease.

In any event, single-system disease with stenosis in the RCA appears to confer better survival than can be expected with LAD disease, at least for 5 years (RCA 96%, LAD 92%). When single-system stenosis is in the LAD, a very proximal location (proximal to the large septal branch) imposes less favorable survival than more distal lesions (proximal 90% at 5 years, distal 98%). Although not conclusively demonstrated, more severe stenoses (>90%), especially those proximal in the artery, probably impose higher time-related mortality than less severe stenoses.

Patients with two-system disease as a heterogeneous group have lower survival than those with single-system stenoses, with 5-year survival of about 88% ( Fig. 7-5, B ). At 15 years, survival is about 56%. When the LAD is one of the two systems, the same effects of location and severity as mentioned for single-system disease pertain. Differences in outcome between single- and two-system disease are not as great as those between two- and three-system disease.

As a heterogeneous group, patients with three-system disease have a 5-year survival without interventional treatment of about 70% ( Fig. 7-5, C ) and a 10- and 15-year survival of about 60% and 40%, respectively. Factors affecting survival in patients with important single-system disease involving the LAD also affect survival in patients with three-system disease. Also, the greater the number of systems with important proximal stenoses, the lower the time-related survival: at 5 years, survival with no, one, two, and three systems with proximal stenoses is 71%, 64%, 51%, and 45%, respectively.

Important left main coronary artery disease imposes an even lower survival: 40% to 60% at 5 years ( Fig. 7-5, D ). Survival falls to about 10% to 26% by 15 years ( Fig. 7-6 ).

Figure 7-6, Nomograms of specific solutions of multivariable risk factor equations illustrating effect of number of coronary artery systems with important stenoses on time-related freedom from cardiac death in patients randomly assigned to initial medical treatment in Veterans Administration randomized trial of chronic stable angina. For this depiction, patients were censored if they crossed over to coronary artery bypass grafting. Values for each risk factor in the specific solutions of the multivariable equation represented by these nomograms are provided in the American College of Cardiology/American Heart Association Joint Task Force Subcommittee on Coronary Artery Bypass Graft Surgery. A5 A, Patients with normal left ventricular (LV) function. B, Patients with importantly impaired LV function. Key: ACC, American College of Cardiology; AHA, American Heart Association; CABG, coronary artery bypass grafting; LM, left main coronary artery disease; SD, systems diseased.

Severity of angina is a surrogate for the basic risk factor of severity of reduction in coronary blood flow reserve ( Fig. 7-7 ). Also, graded exercise testing (GXT) is a surrogate for the basic risk factor of severity of reduced coronary blood flow reserve and is related to outcome events in CAD patients. For example, in the heterogeneous group of patients randomly assigned to initial medical treatment in the European Coronary Surgery Study Group randomized trial, 1-, 5-, and 10-year survival was 94%, 83%, and 71% in patients with a mildly positive GXT but 92%, 77%, and 62% in those with a strongly positive GXT. Similarly, in a study from the CASS Registry, survival at 12 years after medical treatment was substantially lower among patients with a strongly positive GXT (55% for men, 62% for women) than among those with a mildly positive test (75% for men, 82% for women).

Figure 7-7, Nomograms illustrating effect of severity of angina (expressed as Canadian class) on survival in patients randomly assigned to initial medical treatment in the Veterans Administration randomized trial of chronic stable angina (same equation as in Fig. 7-6 ). A, Survival, leaving patients in follow-up evaluation after crossover to coronary artery bypass grafting (CABG) (“intent to treat” analysis). B, Freedom from cardiac death, censoring patients at time of crossover to CABG.

Progression of Coronary Arteriosclerosis

Rate of progression of coronary arteriosclerosis, which could also be termed aggressiveness of the arteriosclerotic process , cannot as yet be examined directly in multivariable risk factor analyses. Its surrogates have appeared in a number of such analyses. The surrogates may be a substitute not solely for one basic risk factor but at times for several factors. Among them are young age at presentation, diabetes, hypertension, and hyperlipidemia.

An important advance has been the demonstration that progression of arteriosclerotic CAD can be slowed, and that regression of some lesions in some circumstances can be initiated by intensive lipid-lowering therapy.

Coronary Arteriosclerotic Plaques

Number of previous episodes of acute MI may be a surrogate for coronary arteriosclerotic plaques as well as for total area (or number) of arteriosclerotic plaques within the coronary arterial tree. Presence of unstable angina and number of recent episodes may likewise be surrogates. In this regard, however, status of the patient's fibrinolytic and disaggregating systems also plays a role. During very active periods, these systems may neutralize the effects of plaque rupture and minimize severity and frequency of unstable angina and acute MI.

Myocardial Scar

To the extent that resting LV dysfunction in patients with CAD is related directly to amount of scar in the myocardium, surrogates for presence and extent of this basic risk factor include number of prior episodes of acute MI, resting LV systolic and diastolic dysfunction (presence and severity) determined by any of several methods, and a history of chronic heart failure.

Reversible ischemia is capable of producing resting LV dysfunction. Myocardial stunning may persist after reversible ischemia has disappeared and result in LV dysfunction. Unfortunately, methods for distinguishing between scar and reversible ischemia, although useful, are neither entirely accurate nor precise. The frequent finding of only a 0.05 to 0.10 increase in preoperatively depressed EF in many patients after CABG suggests that the proportion of LV dysfunction not attributable to myocardial scarring is small.

In CAD patients treated noninterventionally, mild resting LV dysfunction (EF 35%-50%) minimally affects survival, but severe dysfunction (EF < 35%) substantially reduces it. Thus, other factors being equal, 1- and 5-year survival in patients with mild LV dysfunction is about 95% and 80%, respectively, whereas with severe dysfunction it is about 70% and 40%. Good LV function is found more frequently in patients with single-system disease than those with three-system disease ( Table 7-2 ).

Table 7-2
Association of Left Ventricular Systolic Function and Extent of Severe Coronary Artery Disease with 4-Year Survival in Patients Treated Medically a
Recalculated from CASS Registry by Mock and colleagues.
Ejection Fraction Single-System Disease Two-System Disease Three-System Disease
≤ Ratio < n No. % CL (%) n No. % CL (%) n No. % CL (%) P [χ 2 ] b
0.50 761 723 95 94-96 415 386 93 91-94 227 186 82 79-85 <.0001
0.35 0.50 184 167 91 88-93 144 120 83 79-87 88 62 70 65-76 .0001
0.35 57 42 74 66-80 57 32 56 48-64 69 35 51 44-58 .03
P [χ 2 ] <.0001 <.0001 <.0001
Key: CL , 70% confidence limits; n , total patients; No., patients with disease.

a In current era, as estimated by global ejection fraction. Severe disease is 70% or greater reduction in diameter. These data must be interpreted in light of the fact that during the study period, approximately 20%, 30%, and 45% of patients with single-, two-, and three-system disease, respectively, crossed over to surgical treatment.

b P values for difference in predicted survival.

Secondary Conditions

Certain conditions develop secondary to ischemic heart disease and are additional incremental risk factors for death and other unfavorable events.

Hemodynamic Instability

Grade 1 hemodynamic instability is mild and responds to catecholamine infusion. Grade 2 is more severe and responds only when intraaortic balloon pumping is added. Grade 3 is unresponsive even to addition of intraaortic balloon pumping and requires cardiopulmonary support (cardiopulmonary bypass, extracorporeal membrane oxygenation) or a ventricular assist device (see Section I in Chapter 5 ). Because hemodynamic instability in patients with ischemic heart disease typically reflects acute myocardial ischemia or necrosis and produces secondary deleterious effects throughout the body, it adversely affects outcome.

Ischemic Instability

Ischemic instability is a state of unstable angina and implies acute myocardial ischemia. It carries the risk that severe myocardial stunning and necrosis or ischemic ventricular electrical instability can develop acutely.

Ventricular Electrical Instability

Either ischemic or secondary to phenomena associated with myocardial scarring, ventricular electrical instability is a risk factor incremental to that of the basic milieu that gives rise to it.

Coexisting Conditions

Older Age

Older age at presentation is a risk factor for death in patients with ischemic heart disease, and probably acts as a coexisting condition rather than directly affecting CAD.

Diabetes

Diabetes is a strong risk factor for death in CAD patients because of its effect as a coexisting condition and its accelerating effect on the arteriosclerotic process. Fig. 7-8 illustrates the powerful effect of diabetes in elderly patients who have undergone PCI.

Figure 7-8, Nomogram illustrating effect of diabetes on survival after percutaneous coronary intervention (PCI) in elderly patients (same equation as in Fig. 7-6 ).

Hypertension

The strong effect of hypertension as a risk factor for death in CAD patients is related to kidney damage, intracranial complications, LV hypertrophy, and acceleration of the arteriosclerotic process ( Fig. 7-9 ).

Figure 7-9, Nomogram illustrating effect of hypertension on time-related probability of freedom from cardiac death in patients randomly assigned to initial medical treatment in the Veterans Administration randomized trial of chronic stable angina (same equation as in Fig. 7-6 ). Key: CABG, Coronary artery bypass grafting.

Gender

Although overall mortality is lower in women with angina than men, for patients older than 65, relative risks are similar (2.7 vs. 2.4, respectively).

Other Comorbidity

Any serious coexisting disease adversely affects survival in patients with CAD. Of particular importance, because of their prevalence in this group of patients, are chronic obstructive pulmonary disease and chronic renal disease . Smoking can be considered an important coexisting condition.

Technique of Operation

Most patients undergoing CABG have extensive three-system disease, often with important stenoses in four, five, or six arteries. Many have substantial impairment of LV function. This discussion focuses on operation under these circumstances and tactics for accomplishing optimal revascularization and optimal intraoperative management of the myocardium.

Surgical management of arteriosclerotic CAD has evolved from treatment primarily of patients with stable coronary syndromes undergoing elective operation, to treatment of more heterogeneous groups of patients with various clinical syndromes who are older and have more comorbid conditions, including patients who require urgent or emergency operation. Economic and other external pressures often result in CABG being performed within hours after diagnostic coronary angiography or PCI.

At present, CABG with use of total CPB through a full sternotomy remains the most widely used surgical technique. Because of extensive experience, this approach is the technique to which all others must be compared. Other techniques currently in use include CABG through a full sternotomy but without use of CPB, and operations through smaller sternal, parasternal, or thoracotomy incisions with or without use of CPB (see Fig. 2-23 ).

Here, the conventional operation with CPB, as well as the off-pump procedure, are presented. Other procedures are discussed under Special Situations and Controversies later in this chapter.

Preoperative Preparation

Many patients come to CABG taking β-adrenergic receptor or calcium channel blocking agents, angiotensin-converting enzyme (ACE) inhibitors, digitalis preparations, antiarrhythmic agents, and platelet antiaggregating drugs. Some are receiving intravenous heparin and nitroglycerin. It is advisable in most circumstances to continue β-adrenergic receptor and calcium channel blockers, as well as ACE inhibitors, up to the time of operation (see “Management of Preoperative Medications” in Section I of Chapter 4 ). Several studies have shown a tendency toward development of acute MI in patients in whom β-adrenergic receptor agents are discontinued. Boudoulas and colleagues demonstrated an important increase in adrenergic tone in most patients the day before operation that could be reduced by propranolol. Propranolol has also been shown to lessen prevalence of intraoperative ventricular arrhythmias without compromising LV function in low or moderate dosages. Patients receiving preoperative β-adrenergic receptor agents, amiodarone, or sotalol are less likely to develop atrial fibrillation postoperatively.

Digitalis preparations can be discontinued preoperatively unless atrial fibrillation is present (see Chapter 4 ). They can be administered intraoperatively and postoperatively for control of heart rate if atrial fibrillation or other atrial arrhythmias are present.

Platelet antiaggregating drugs such as abciximab, eptifibatide, tirofiban, clopidogrel, prasugrel, and ticagrelor bind to the glycoprotein IIb/IIIa platelet receptors. When feasible, these drugs as well as aspirin should be discontinued at the appropriate time interval before operation (each has a different half-life) if the patient has a stable coronary syndrome, because their use is associated with increased postoperative bleeding and need for transfusion of blood products.

Patients who have received plasminogen-activating (fibrinolytic) agents such as streptokinase, alteplase, and reteplase preoperatively require careful attention intraoperatively and postoperatively to manage excessive bleeding.

Operating Room Preparation

Anesthetic methods for CABG are described in Chapter 4 . After inserting an endotracheal tube and appropriate monitoring devices (see Chapter 2 ), the skin is prepared over the chest, abdomen, groin, one or both arms if indicated, and the complete circumference of both legs, including the feet. Draping includes isolating the feet, genitalia, and pubis and placing sterile waterproof drapes beneath the legs.

Surgical Strategy

The prime objective of CABG is to obtain complete revascularization by bypassing all severe stenoses (at least 50% diameter reduction) in all coronary arterial trunks and branches having a diameter of about 1 mm or more. Because five or more individual conduits cannot be conveniently used in most patients, at least some of the grafts may require sequential (side-to-side) anastomoses. To increase the likelihood that the entire graft will remain patent, the distal end-to-side anastomosis of a sequential graft should be made, whenever possible, to a relatively large artery with a substantial proximal stenosis and good runoff. Although it is not clearly established whether grafts with more than one distal anastomosis have the same, higher, or lower patency rates than those with only a single distal anastomosis, several studies suggest that sequential grafts are associated with higher mean flows and graft patency. As a general principle, conservation of conduit by employing sequential grafting is prudent because of the likelihood of subsequent CABG or peripheral arterial procedures that may require use of saphenous vein grafts.

A widely used strategy involves routine use of the left ITA to the LAD and segments of saphenous vein to the remaining coronary arteries requiring revascularization. The right ITA, one or both radial arteries, and the right gastroepiploic artery can also be used in combination with the left ITA. Sequential anastomoses with the ITA and radial artery can be performed with satisfactory results. Figs. 7-10 and 7-11 show the most widely used combinations and configurations of bypass grafts. Details of graft placement are often individualized according to location and severity of arteriosclerotic disease, surgeon preference, availability of suitable conduit, and knowledge of the long-term function of various conduits.

Figure 7-10, Combinations and configurations of saphenous vein bypass grafts. A, Vein graft is anastomosed side to side to a diagonal branch of left anterior descending coronary artery (LAD) and end to side to LAD. B, In circumflex system, vein graft is anastomosed side to side to one or more proximal marginal branches and end to side to most distal marginal branch. C, Sequential grafts to circumflex system (Cx) can be extended to include branches of right coronary artery (RCA). D, In RCA system, vein graft can be anastomosed side to side to posterior descending coronary artery and end to side to one or more left ventricular branches of RCA. E, Sequential grafts to RCA system can be extended to include branches of Cx artery. Direction of a sequential graft to RCA and Cx artery systems (configuration C or E ) is chosen so that the largest coronary artery branch is placed at end of sequence.

Figure 7-11, Combinations and configurations of internal thoracic artery (ITA) bypass grafts. A, Left ITA is most often used to bypass the left anterior descending coronary artery (LAD). B, Sequential grafting using left ITA may include a diagonal branch of LAD. C, Right ITA can be used to bypass right coronary artery (RCA) alone or in combination with an ITA graft to LAD system. D, Alternatively, right ITA can be passed through transverse sinus and anastomosed to one or more marginal branches of left circumflex coronary artery. E, Right ITA can be brought across midline and used to bypass LAD, and if indicated, left ITA can be anastomosed to one or more marginal branches of left circumflex coronary artery. F, When extensive revascularization of posterior wall of left ventricle (LV) is required, a posteriorly positioned sequential vein graft (or radial artery) in combination with a left ITA graft to the LAD is typically used. G, Radial artery graft may be used as a sequential graft to bypass arteries on lateral and posterior surfaces of LV. Radial artery can be anastomosed proximally to left ITA, which is used to bypass the LAD. Alternatively, radial artery can be anastomosed directly to ascending aorta. H, Right gastroepiploic artery or splenic artery may be used to bypass branches of right and circumflex coronary arteries in combination with ITA or other grafts to LAD circulation.

The cineangiogram provides key information for planning CABG, but based on either the cineangiogram or observations made at operation, the surgeon may elect to open vessels suspected of having important stenosis. A few errors will inevitably be made regarding which vessels should be grafted. The surgeon must decide which error is more acceptable: opening and grafting an artery that does not need it or failing to open and graft a vessel with an important stenosis. The latter is generally considered a more serious error.

Coronary Artery Bypass Grafting

With Cardiopulmonary Bypass

A median sternotomy is made, and at the same time a segment of greater saphenous vein (or radial artery or other conduit) is removed. Before the pericardium is opened, the left ITA (and the right if indicated) is completely mobilized. Heparin is administered as dissection of the ITA is being completed. The ITA is then divided. A bulldog clamp or clip is placed on the artery near the open end, and the distal segment of the artery on the chest wall is ligated or clipped. The pericardium is opened, and pericardial stay sutures are placed. Purse-string sutures are placed at the sites for cannulation and also in the ascending aorta and right atrial wall for controlled aortic root perfusion and delivery of cardioplegia into the coronary sinus (see Fig. 2-22 ). Because arteriosclerosis is frequently present in the ascending aorta and proximal aortic arch in patients with CAD, particularly elderly patients, epiaortic ultrasonographic scanning of the aorta is advisable before aortic cannulation to obtain information that can lead to safe positioning of cannulae and aortic clamps (see “Epiaortic Ultrasonography” in Chapter 26 ).

CPB is established using a single venous cannula. Catheters for administering cardioplegic solution are placed into the ascending aorta and coronary sinus through the previously placed purse-string sutures and secured with tourniquets. The aorta is clamped and cardioplegic solution infused (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). The heart can be covered with cold saline during administration of cold cardioplegia to facilitate cooling.

With the heart retracted out of the pericardial cavity and toward the head of the patient by an assistant standing to the surgeon's left or by traction sutures placed on the acute margin of the heart, the first anastomosis of the conduit that has been selected is made to the distal RCA or to the posterior descending artery (PDA) (see Fig. 7-10, D ). (See “ Distal Anastomosis ” later in this chapter.) Sequential anastomoses of the conduit can be performed to more distal branches of the RCA or to the marginal branches of the Cx coronary artery (see Fig. 7-10, E ). The graft is then distended gently with cardioplegic solution, positioned along the right atrium up to the right side of the ascending aorta, and transected at the point that will permit a smooth course of the conduit without kinking or tension. The free end of the graft is spatulated.

The heart is then retracted to the right by the assistant. A separate conduit is anastomosed to one or more of the marginal branches of the Cx artery (see Fig. 7-10, B ). The graft is properly oriented to avoid twisting, and the heart is repositioned in the pericardial cavity. The graft is distended gently with cardioplegic solution, cut to the appropriate length, and spatulated. This graft can be positioned anterior to the pulmonary artery or passed through the transverse sinus for anastomosis to the right side of the aorta. A third segment of conduit can be anastomosed to one or more diagonal branches of the LAD. This segment can be brought anterior to the pulmonary artery or through the transverse sinus.

The ITA is cut to the appropriate length, and a bulldog clamp is placed on the proximal portion. If the operation has been performed using hypothermia, rewarming is begun at this time. The pericardium is incised widely to permit proper alignment of the ITA with the LAD and its diagonal branches, taking care to avoid injury to the left phrenic nerve. A pad is placed beneath the LV, and the LAD is isolated and incised. The distal end of the ITA is spatulated and sutured to the LAD and sequentially to a diagonal branch of the LAD if indicated (see Fig. 7-11, A and B ).

The aortic clamp is removed, a partially occluding clamp is placed on the ascending aorta, and two or three openings are made with a punch in the isolated aortic segment. The grafts are sutured to the aorta so that they are free of kinking or tension. If grafts have been passed through the transverse sinus, they are anastomosed to openings made on the right lateral surface of the ascending aorta. Because of increasing evidence implicating the arteriosclerotic ascending aorta as an important source of emboli to the brain and other organs, it may be preferable to avoid placing the partially occluding clamp on it and to perform the proximal anastomoses during a single period of aortic clamping with the heart arrested.

The partially occluding clamp (or the aortic clamp if a partially occluding clamp has not been used) is then removed. Air is evacuated from the ascending aorta, and controlled aortic reperfusion, if indicated, is begun. Once rewarming has been completed and the heart is beating well, CPB is discontinued and cannulae are removed. Temporary atrial and ventricular pacing wires and chest drainage tubes are placed. Remainder of operation is completed in the standard manner (see “Completing Cardiopulmonary Bypass” in Section III of Chapter 2 ).

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